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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2745_Библиотеки_им_академика_М_И_Перельмана
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Chronic small vessel ischemic disease yields subtle white
matter degradation that can be difficult to distinguish from
low-grade MS-related inflammation both radiologically and
cognitively. In both cases, MRI can show periventricular white
matter change, and patients tend to present cognitively with
mildly slowed information processing speed and subtle forms
of executive dysfunction. Widespread cerebral hypoperfusion
has been implicated as a possible mechanism for cognitive
dysfunction in MS as well.
95
With advances in effective disease-modifying therapies, MS
patients continue to live longer. Older adults with MS must
contend with normal age-related cognitive change and
disorders such as Alzheimer disease (AD). The public
awareness of AD makes it a source of concern for many
individuals, particularly those perceiving cognitive changes in
themselves or family members. To conclusively rule in or out
an AD diagnosis, there is no substitute for complete
neurological evaluation, aided by structural/functional
neuroimaging and neuropsychological testing. Nonetheless,
there are several identifying features which can help the
clinician determine whether AD is likely, and put the patient’s
mind at ease when it is not.
Age is the most significant AD risk factor, with incidence
highest after age 65 years and increasing dramatically with
each subsequent decade of life. Genetic factors also play a
role, and several primary genes have been identified in
association with AD development. Nonetheless, greater than
95% of AD cases are of the sporadic variant and tend to follow
a later-onset course. 96 Early-onset AD, defined alternately in
research by presentation before either age 60 or 65 years, is
uncommon and is strongly associated with mutation in three
specific genes, rarely occurring in the absence of such familial
risk. 97 Accordingly, MS patients under the age of 60 years
should be counseled that their cognitive complaints are not
likely indicative of AD. Furthermore, even patients with a
family history of AD should know that this only slightly
increases their risk of AD development and is by no means a
guarantee that they will eventually develop a dementia.
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The MS neurocognitive profile, involving subcortical
dysfunction, also tends to be more subtle and less specific than
the cortical disruption seen in AD. While MS patients
demonstrate reduced processing speed and difficulties learning
new information, the hallmarks of AD are reductions in
language and retrieval of both recent and distant memories.
While both MS and AD cognitive dysfunction may lead to
complaints by patients, the overt loss of language and
generally poor memory in AD can be more noticeable to
friends, family, and coworkers.
Severity of cognitive impairment is often defined by the extent
to which it interferes with a patient’s day-to-day functioning.
However, loss of independence due to physical disability, as is
common in MS, should not be conflated with inability to
perform essential cognitive tasks. Although the latter does
occur in MS, patients often maintain the ability to care for
themselves given appropriate compensatory aids. By contrast,
patients with AD frequently progress to a point where they
cannot safely engage in self-care due to their cognitive
impairment.
Finally, the course of onset is important clinical evidence. AD
pathology is insidious and progressive, and associated
cognitive deficits emerge in the same manner. As noted
previously, MS-related cognitive dysfunction is often linked to
the presence of new inflammatory events or other signs of
increased disease activity. For patients with the relapsingremitting MS subtype, the presence of stepwise cognitive
changes, particularly when temporally related to inflammatory
events, represents a considerable distinction from the
consistent worsening of cognition over time in AD and other
progressive dementias. Furthermore, cognitive changes do not
remit after onset in AD but may do so partially or fully in MS,
particularly during quiescent periods of disease or in direct
response to MS treatment. In general, a second diagnosis of
AD or another progressive dementia should only be made
when there is sufficient evidence of an additional disease
process beyond MS; otherwise, it is more likely that cognitive
changes can be attributed to a preexisting MS diagnosis.
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Numerous other medical conditions with high comorbidity to
MS are associated with onset or exacerbation of cognitive
symptoms. Seizure disorders occur in approximately three
percent of MS patients, 98 and presence of seizures is
associated with higher rate of subcortical white matter lesions.
99
Autoimmune thyroid disease, associated with fluctuations in
cognitive performance and energy level, occurs in more than
six percent of MS patients.
100
This list is by no means
exhaustive, and the presence of any other significant medical
comorbidities should be taken into account when assessing the
etiology of cognitive complaints in patients with MS.
Treatment and Intervention
Development and validation of empirical treatments for MSrelated cognitive dysfunction is an active area of research, but
it remains a work in progress. Early monitoring of cognitive
impairment should be considered a priority, as research
suggests that cognitive decline may accelerate after an initial
period, providing a window for intervention to begin promptly.
37,101
Adherence to disease-modifying therapy and prevention of MS
progression may be the best way to prevent cognitive decline,
as pharmacological interventions targeted specifically at
cognitive symptoms have not yet demonstrated significant
effectiveness.
102-104
Cognitive rehabilitation protocols are
under development, with mixed initial results. Several
systematic reviews have found limited evidence for cognitive
rehabilitation programs, though statistical comparisons were
made difficult by heterogeneous research methodology across
studies.
105-108
There are two class I randomized controlled
trials (RCTs) providing good evidence that verbal learning and
memory can be improved in MS.
109,110
Both studies
demonstrated accompanying functional MRI (fMRI) cerebral
activation data as supporting evidence.
110,111
Improvements in
the former study were maintained at 6-month follow-up. In
addition, there is some mixed evidence that attention can be
improved with computerized cognitive rehabilitation program.
112
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An important theoretical basis of cognitive training programs
is enhancement of cognitive reserve, the resilience of the mind
to brain disease. Patients with stronger cognitive ability before
the onset of disease are not only less likely to fall below the
threshold for normal cognition but are generally more resistant
to experiencing significant decline from their personal
cognitive baseline.
113,114
Level of education is the best-known
predictor of cognitive reserve,
115
although vocational status
and premorbid engagement in intellectually stimulating leisure
activities also appear relevant.
116-118
Additional research is
needed to determine whether these links are solely
correlational and manifest only in the premorbid phase of
illness or whether behavioral changes can induce greater
cognitive resilience after disease onset.
119
Physical exercise programs have general health benefits, and
there is preliminary evidence that aerobic exercise may
improve memory in MS patients.
120,121
To encourage safety,
driving evaluations may be indicated in patients with deficits
in processing speed, attention, or visual-spatial ability, which
can impact driving ability.
122
Addressing fatigue, mood, and
physical health can also be beneficial to functional cognitive
performance. Pending the outcome of further intervention
trials, current best practices include using evidence-based
interventions for memory and attention, as well as provision of
supportive therapy and teaching of compensatory strategies for
impaired cognitive functions in general.
123
Summary
Cognitive dysfunction is highly prevalent among MS patients
and is a prominent aspect of the MS disability profile. Changes
in cognition are associated with poorer quality of life,
decreased capacity to work and engage socially, and loss of
independence. Processing speed is the primary cognitive
deficit in MS, but it can manifest in ways other than
generalized slowing. Patients may also complain of problems
with memory, attention, language, visual-spatial processing, or
executive functioning, and the heterogeneity of disease
progression and focal nature of central nervous system lesions
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allow for the possibility of impairment in any cognitive
domain. The best way to elucidate the nature and severity of
cognitive deficits is through formal neuropsychological
evaluation, and recent developments in MS-specific cognitive
assessment have improved methods for screening and
longitudinal monitoring of cognition.
Etiological considerations for cognitive impairment in MS are
multifactorial and include the direct consequences of disease
activity, fatigue, medication effects, psychological stressors,
and other medical conditions that may influence cognitive
ability. Efforts to develop effective cognitive rehabilitation
protocols are ongoing. There is some class I evidence for
improvements in verbal memory, preliminary evidence for
improvements in attention, and evidence in favor of supportive
therapy and teaching of compensatory skills for cognitive
impairment in general. More importantly, educating patients,
clinicians, and caregivers about the frequency and impact of
cognitive change in MS is an important step toward addressing
this critical area of disability.
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